UVB radiation exposure modulates mitophagy in embryonic cells of freshwater prawn Macrobrachium olfersii: Exploring a protective organelle quality control mechanism

IF 4.6 Q2 MATERIALS SCIENCE, BIOMATERIALS
Giuliam K. Strücker , Michael L. Jaramillo , Thaline de Quadros, Evelise M. Nazari
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Abstract

Aquatic environments are subject to ultraviolet B (UVB) radiation incidence, and its effects on organisms are dose-dependent. Besides DNA, mitochondria are an important target of this radiation that causes structural damage and impairs its functional dynamics. Here, we hypothesize that mitophagy acts as an organelle quality control mechanism to mitigate UVB impacts in embryonic cells. Then, freshwater prawn Macrobrachium olfersii embryos was used as a model to investigate the effects of UVB on genes (Tomm20, Opa1, Pink, Prkn, Sqstm1, and Map1lc3) and proteins (TOM20, PINK1, p62 and LC3B) involved in mitophagy modulation. The choice of genes and proteins was based on the identification of mitochondrial membrane (Tomm20, Opa1 and TOM20), mediation of mitophagy (Pink1, Prkn and PINK1), and recognition of mitochondria by the autophagosome membrane (Sqstm1, Map1lc3, p62 and LC3B). First, the phylogeny of all genes presented bootstrap values >80 and conserved domains among crustacean species. Gene expression was inherently modulated during development, with transcripts (Tomm20, Opa1, Pink, Prkn, Sqstm1, and Map1lc3) overexpressed in the initial and final stages of development. Moreover, UVB radiation induced upregulation of Tomm20, Opa1, Pink, Prkn, Sqstm1, and Map1lc3 genes at 6 h after exposure. Interestingly, after 12 h, the protein content of PINK1, p62, and LC3B increased, while TOM20 was not responsive. Despite UVB radiation's harmful effects on embryonic cells, the chronology of gene expression and protein content indicates rapid activation of mitophagy, serving as an organelle quality control mechanism, given the analyzed cells' integrity.

Abstract Image

紫外线辐射调节淡水对虾胚胎细胞的有丝分裂:探索一种保护性细胞器质量控制机制
水生环境受到紫外线 B(UVB)辐射的影响,其对生物的影响与剂量有关。除了 DNA 外,线粒体也是这种辐射的一个重要目标,辐射会造成线粒体结构损伤并损害其功能动态。在此,我们假设线粒体吞噬是一种细胞器质量控制机制,可减轻紫外线对胚胎细胞的影响。我们以淡水对虾(Macrobrachium olfersii)胚胎为模型,研究了紫外线对参与有丝分裂调控的基因(Tomm20、Opa1、Pink、Prkn、Sqstm1和Map1lc3)和蛋白(TOM20、PINK1、p62和LC3B)的影响。基因和蛋白质的选择基于对线粒体膜(Tomm20、Opa1 和 TOM20)、有丝分裂中介(Pink1、Prkn 和 PINK1)以及自噬体膜对线粒体的识别(Sqstm1、Map1lc3、p62 和 LC3B)的鉴定。首先,所有基因的系统进化都呈现出引导值大于 80 的结果,并且在甲壳类物种之间呈现出保守的结构域。基因表达在发育过程中受到内在调控,转录本(Tomm20、Opa1、Pink、Prkn、Sqstm1和Map1lc3)在发育初期和末期过度表达。此外,紫外线辐射在照射 6 小时后诱导 Tomm20、Opa1、Pink、Prkn、Sqstm1 和 Map1lc3 基因上调。有趣的是,12小时后,PINK1、p62和LC3B的蛋白含量增加,而TOM20却没有反应。尽管紫外线辐射对胚胎细胞有害,但基因表达和蛋白质含量的时间顺序表明,有丝分裂迅速被激活,鉴于所分析细胞的完整性,有丝分裂是一种细胞器质量控制机制。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
ACS Applied Bio Materials
ACS Applied Bio Materials Chemistry-Chemistry (all)
CiteScore
9.40
自引率
2.10%
发文量
464
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